Kos D, Kerckhofs E, Nagels G, D'hooghe M B, Ilsbroukx S
Vrije Universiteit Brussel, Department of Rehabilitation Research, Brussels, Belgium.
Neurorehabil Neural Repair. 2008 Jan-Feb;22(1):91-100. doi: 10.1177/1545968306298934. Epub 2007 Apr 4.
Fatigue is one of the most common and most disabling symptoms of multiple sclerosis (MS). Although numerous studies have tried to reveal it, no definite pathogenesis factor behind this fatigue has been identified. Fatigue may be directly related to the disease mechanisms (primary fatigue) or may be secondary to non-disease-specific factors. Primary fatigue may be the result of inflammation, demyelination, or axonal loss. A suggested functional cortical reorganization may result in a higher energy demand in certain brain areas, culminating in an increase of fatigue perception. Higher levels of some immune markers were found in patients with MS-related fatigue, whereas other studies rejected this hypothesis. There may be a disturbance in the neuroendocrine system related to fatigue, but it is not clear whether this is either the result of the interaction with immune activation or the trigger of this process. Fatigue may be secondary to sleep problems, which are frequently present in MS and in their turn result from urinary problems, spasms, pain, or anxiety. Pharmacologic treatment of MS (symptoms) may also provoke fatigue. The evidence for reduced activity as a cause of secondary fatigue in MS is inconsistent. Psychological functioning may at least play a role in the persistence of fatigue. Research did not reach consensus about the association of fatigue with clinical or demographic variables, such as age, gender, disability, type of MS, education level, and disease duration. In conclusion, it is more likely to explain fatigue from a multifactor perspective than to ascribe it to one mechanism. The current evidence on the pathogenesis of primary and secondary fatigue in MS is limited by inconsistency in defining specific aspects of the concept fatigue, by the lack of appropriate assessment tools, and by the use of heterogeneous samples. Future research should overcome these limitations and also include longitudinal designs.
疲劳是多发性硬化症（MS）最常见且最致残的症状之一。尽管众多研究试图揭示其原因，但尚未确定导致这种疲劳的确切发病机制因素。疲劳可能与疾病机制直接相关（原发性疲劳），也可能继发于非疾病特异性因素。原发性疲劳可能是炎症、脱髓鞘或轴突损失的结果。一种推测的功能性皮质重组可能导致某些脑区能量需求增加，最终导致疲劳感增强。在患有MS相关疲劳的患者中发现了一些免疫标志物水平较高，而其他研究则否定了这一假设。可能存在与疲劳相关的神经内分泌系统紊乱，但尚不清楚这是与免疫激活相互作用的结果还是这一过程的触发因素。疲劳可能继发于睡眠问题，而睡眠问题在MS中很常见，反过来又由泌尿系统问题、痉挛、疼痛或焦虑引起。MS的药物治疗（症状）也可能引发疲劳。关于活动减少作为MS继发性疲劳原因的证据并不一致。心理功能至少可能在疲劳的持续存在中起作用。关于疲劳与临床或人口统计学变量（如年龄、性别、残疾程度、MS类型、教育水平和病程）之间的关联，研究尚未达成共识。总之，从多因素角度解释疲劳比将其归因于一种机制更有可能。目前关于MS原发性和继发性疲劳发病机制的证据受到以下因素的限制：疲劳概念特定方面定义的不一致、缺乏适当的评估工具以及使用异质性样本。未来的研究应克服这些局限性，还应包括纵向设计。
